Otitis Media

Author: Muhammad Waseem, MD; Chief Editor: Glenn C Isaacson, MD, FACS, FAAP

Background
Otitis media (OM) is the second most common disease of childhood, after upper respiratory infection
(URI). OM is also the most common cause for childhood visits to a physician's office. Annually, an
estimated 16 million office visits are attributed to OM; this does not include visits to the emergency
department.
OM is any inflammation of the middle ear without reference to etiology or pathogenesis. OM can be
classified into many variants on the basis of etiology, duration, symptomatology, and physical findings.
Acute OM (AOM) implies rapid onset of disease associated with one or more of the following symptoms:
Otalgia
Fever
Otorrhea
Recent onset of anorexia
Irritability
Vomiting
Diarrhea
These symptoms are accompanied by abnormal otoscopic findings of the tympanic membrane (TM),
which may include the following:
Opacity
Bulging
Erythema
Middle ear effusion (MEE)
Decreased mobility with pneumatic otoscopy
AOM is a recurrent disease. More than one third of children experience 6 or more episodes of AOM by
age 7 years.
OM with effusion (OME), formerly termed serous OM or secretory OM, is MEE of any duration that lacks
the associated signs and symptoms of infection (eg, fever, otalgia, irritability). OME usually follows an
episode of AOM.
Chronic suppurative OM is a chronic inflammation of the middle ear that persists at least 6 weeks and is
associated with otorrhea through a perforated TM, an indwelling tympanostomy tube (TT; see image
below), or a surgical myringotomy.

Various tympanostomy tube styles and sizes.

Pathophysiology
The most important factor in middle ear disease is eustachian tube (ET) dysfunction. In ET dysfunction
(ETD), the mucosa at the pharyngeal end of the ET is part of the mucociliary system of the middle ear.
Interference with this mucosa by edema, tumor, or negative intratympanic pressure facilitates direct
extension of infectious processes from the nasopharynx to the middle ear, causing OM. Esophageal
contents regurgitated into the nasopharynx and middle ear through the ET can create a direct mechanical
disturbance of the middle ear mucosa and cause middle ear inflammation.
In children, developmental alterations of the ET, an immature immune system, and frequent infections of
the upper respiratory mucosa all play major roles in AOM development. Studies have demonstrated how
viral infection of the upper respiratory epithelium leads to increased ETD and increased bacterial
colonization and adherence in the nasopharynx. [1] Certain viral infections cause abnormal host immune
and inflammatory responses in the ET mucosa and subsequent microbial invasion of the middle ear. The

host immune and inflammatory response to bacterial invasion of the middle ear produces fluid in the
middle ear and the signs and symptoms of AOM.
Although interactions between the common pathogenic bacteria in AOM and certain viruses are not fully
understood, strong evidence indicates that these interactions often lead to more severe disease, lowered
response to antimicrobial therapy, and OME development following AOM.

Epidemiology
Frequency
United States
OM, the most common specifically treated childhood disease, accounts for approximately 20 million
annual physician visits. Various epidemiologic studies report the prevalence rate of AOM to be 17-20%
within the first 2 years of life, and 90% of children have at least one documented MEE by age 2 years.
OM is a recurrent disease. One third of children experience 6 or more episodes of AOM by age 7 years.
International
Incidence and prevalence in other industrialized nations are similar to US rates. In less developed
nations, OM is extremely common and remains a major contributor to childhood mortality resulting from
late-presenting intracranial complications.

Mortality/Morbidity
US mortality rates are extremely low in this era of antimicrobial therapy (< 1 death per 100,000 cases). In
developing nations with limited access to primary medical care and modern antibiotics, mortality rates are
similar to US rates before antibiotic therapy. A study that examined the causes of death in Los Angeles
County Hospital from 1928-1933, years prior to the advent of sulfa, showed 1 in 40 deaths was caused by
intracranial complications of OM.
Morbidity from this disease remains significant, despite frequent use of systemic antibiotics to treat the
illness and its complications. Intratemporal and intracranial complications of OM are the 2 major types.
Intratemporal complications
o Hearing loss (conductive and sensorineural)
o TM perforation (acute and chronic)
o Chronic suppurative OM (with or without cholesteatoma)
o Cholesteatoma
o Tympanosclerosis
o Mastoiditis
o Petrositis
o Labyrinthitis
o Facial paralysis
o Cholesterol granuloma
o Infectious eczematoid dermatitis
Intracranial complications
o Meningitis
o Subdural empyema
o Brain abscess
o Extradural abscess
o Lateral sinus thrombosis
o Otitic hydrocephalus

Race
Until recently, prevalence of OM in the United States was reported to be higher in black and Hispanic
children than in white children. A study that controlled for socioeconomic and other confounding factors
showed equal incidence in blacks and whites. Hispanic children and Alaskan Inuit and other American
Indian children have higher prevalence of AOM than white and black children in the United States.
International studies show increased prevalence of AOM and chronic OM (COM) among Micronesian and
Australian aboriginal children.

Sex
Several more recent studies have shown equal AOM prevalence in males and females; many previous
studies had shown increased incidence in boys.

Age

Peak prevalence of OM in both sexes occurs in children aged 6-18 months.

Some studies show bimodal prevalence peaks; a second, lower peak occurs at age 4-5 years
and corresponds with school entry.
Although OM can occur at any age, 80-90% of cases occur in children younger than 6 years.
Children who are diagnosed with AOM during the first year of life are much more likely to develop
recurrent OM and chronic OME than children in whom the first middle ear infection occurs after
age 1 year.

History

Suspect acute otitis media (AOM), with or without effusion, in children with a history of the
following symptoms:
o Head and neck
Otalgia: Young children may exhibit signs of otalgia by pulling on the affected ear
or ears or pulling on the hair. Otalgia apparently occurs more often when the
child is lying down (eg, during the night, during nap time), which may be due to
increased ETD when the child is in a recumbent position.
Otorrhea: Discharge may come from the middle ear through a recently perforated
TM, through a preexisting TT, or through another perforation. For trauma
patients, excluding a basilar skull fracture with associated cerebrospinal fluid
(CSF) otorrhea is important.
Headache
Concurrent or recent URI symptoms (eg, cough, rhinorrhea, sinus congestion)
o General
Two thirds of children with AOM have a history of fever, although fevers greater
than 40C are uncommon and may represent bacteremia or other complications.
Irritability may be the sole early symptom in a young infant or toddler.
A history of lethargy, although nonspecific, is a sensitive marker for sick children
and should not be dismissed.
o GI tract: Symptoms include anorexia, nausea, vomiting, and diarrhea.
OME often follows an episode of AOM. Consider OME in patients with recent AOM in whom the
history includes any of the following symptoms:
o Hearing loss: Most young children cannot provide an accurate history. Parents,
caregivers, or teachers may suspect a hearing loss or describe the child as inattentive.
o Tinnitus: This is possible, although it is an unusual complaint from a child.
o Vertigo: Although true vertigo (ie, room-spinning dizziness) is a rare complaint in
uncomplicated AOM or OME, parents may report some unsteadiness or clumsiness in a
young child with AOM.
o Otalgia: Intermittent otalgia tends to worsen at night.
OM treatment widely varies based on the duration of symptoms, past therapeutic failures, and
severity of current symptoms.
Exposure to environmental risk factors is another important aspect of the history and includes the
following:
o Passive exposure (ie, secondhand) to tobacco smoke
o Group daycare attendance
o Seasonality: AOM prevalence is much higher in winter and early spring than in summer
and early fall.

Supine bottle feeding (ie, bottle propping)

Physical
Pneumatic otoscopy remains the standard examination technique for patients with suspected OM. When
performed correctly, this technique is 90% sensitive and 80% specific for diagnosis of AOM, and findings
are more accurate than with myringotomy. Proper pneumatic otoscopy technique is crucial to distinguish
AOM from OME because recommended therapies for these entities are significantly different. Studies
show that most practitioners improperly perform otoscopic examinations. Almost one half of physicians
never use pneumatic compression of the TM during routine otoscopic examination, and almost 30% use
otoscopes with inadequate light sources.
Tympanometry, acoustic reflectometry, and audiometry are important adjunctive techniques with which to
evaluate patients with MEE.
In addition to a carefully documented examination of the external ear and TM, examining the entire head
and neck region of patients with suspected OM is important. Several congenital syndromes, craniofacial
anomalies, and systemic diseases have increased incidence associated with OM, including cleft palate,
Down syndrome, Treacher Collins syndrome (ie, mandibulofacial dysotosis), hemifacial microsomia,
diabetes mellitus, human immunodeficiency virus (HIV) infection, and many types of
mucopolysaccharidosis.
Below are examination techniques used in the diagnosis of OM.

Pneumatic otoscopy examination

Under direct visualization, first remove any cerumen, which causes a limited and sometimes
inaccurate view of the TM and inaccurate and confusing results on tympanometry and
audiometry.
To move the TM, the ear speculum must create an air seal against the external auditory canal
(EAC), which is seldom possible with a standard disposable speculum. All otoscope
manufacturers sell inexpensive cuffed ear speculums to perform insufflation. A rubber sleeve over
the speculum may reduce patient discomfort during the examination. Usually, the TM is in the
neutral position (ie, neither retracted nor bulging), pearly gray, translucent, and unperforated. It
responds briskly to positive and negative pressure, indicating an air-filled space. Many older texts
emphasize a TM "light reflex" in an otherwise normal ear. Because this reflex may be absent in
entirely normal ears and present in ears with MEE, the light reflex does not help confirm or
exclude an OM diagnosis.
Every examination should include an evaluation and description of the following 4 TM
characteristics:
o Color
A normal TM is a translucent pale gray.
An opaque yellow or blue TM is consistent with MEE.
Dark red indicates a recent trauma or blood behind the TM.
A dark pink or lighter red TM is consistent with AOM or hyperemia of the TM
caused by crying, coughing, or nose blowing.
Color of the eardrum is less important diagnostically than its position and mobility.
Redness of the TM alone does not necessarily suggest AOM because crying,
removal of cerumen with associated irritation of the auditory canal, coughing,
nose blowing, and fever can all cause redness of the eardrum without a middle
ear infection. Note that most children cry when their ears are examined.
A study of 85 infants showed that the otoscopic finding most predictive of AOM
was a poorly mobile, bulging, yellow, and opacified TM. However, this
appearance was noted in only 19% of patients. In another analysis, a slightly red
TM in a normal position and with normal mobility had a predictive value of only
7% for AOM.
o Position: The position of the TM (ie, bulging, retracted, neutral, full) is key to
differentiating AOM from OME.
In AOM, the TM is usually bulging.

In OME, the TM is typically retracted or in the neutral position.

Mobility: Abnormal movement of the TM during pneumatic otoscopy can suggest various
conditions or disorders.
Movement during negative pressure only suggests ETD.
A TM that moves only slightly with both positive and negative pressure applied
indicates the probable presence of middle ear fluid.
No movement occurs with a TM perforation or a TT.
Studies show that the most consistent physical finding in patients with OME is
impaired mobility of the TM during pneumatic otoscopy. Pay special attention to
movement of retracted segments of the TM because immobility of these sections
may indicate middle ear cholesteatoma in the retraction pockets.
Perforation
Single perforations are most common, but some patients may have multiple
perforations.
Note the location and cause of the perforation.
Perforations in the posterosuperior quadrant, which are the most difficult to
detect, are important because they occasionally are associated with
cholesteatoma.
Pus or other fluid may drain through a perforation.
Multiple perforations and otorrhea that does not yield pathogens on culture may
indicate tuberculosis.

Adjunctive screening techniques for OM: Adjunctive techniques help identify patients with
asymptomatic OME, which may comprise 10% of cases.
Tympanometry (ie, impedance audiometry), the most commonly used adjunctive technique,
measures changes in acoustic impedance of the TM/middle ear system with air pressure changes
in the EAC.
o Current recommendations call for screening tympanometry at the beginning of school
and 1 year later to identify children aged 4-6 years with asymptomatic OME.
o Tympanometry screening has a high degree of sensitivity (>90%) but is not specific for
OME.
o The test may yield false-positive results in children with a retracted TM or a thickened TM
without effusion. Screening tests may also yield invalid results in children who have
cerumen obstructing the external canal or who are crying during the examination.
o Middle ear pressure more than 200 daPa or a flat tympanometric curve is classified as a
failure.
o Further physician evaluation is indicated in a child in whom tympanometry screening fails
in both ears and who has at least a 20-dB hearing loss at 1, 2, or 4 kHz.
o After 2 months, retest any child in whom tympanometry screening fails in one ear and
hearing loss occurs (>20 dB). Also retest children in whom tympanometry screening fails
in both ears, even without marked hearing loss (ie, < 20 dB). A second screening failure
should lead to physician evaluation. Assess the child's hearing, speech, and language
and immediately start therapy to correct deficits.
Acoustic reflectometry uses an acoustic otoscope to measure reflected sound from the TM; the
louder the reflected sound, the greater the likelihood of an MEE. The breakpoint is defined as the
level of sound reflectivity that correlates with the presence of MEE.
o Acoustic reflectometry is rapid and easy to perform. Among its advantages over
tympanometry is that an airtight seal of the EAC is unnecessary and that the test is
unaffected by a crying patient or the presence of cerumen in the EAC.
o Despite these advantages, acoustic reflectometry has not been widely accepted by
otolaryngologists because of the difficulty in setting standards to interpret test results.
o No accepted breakpoint standards have been established, so sensitivity and specificity
vary according to the breakpoints set for each study. A low breakpoint leads to high

sensitivity but low specificity. A high breakpoint leads to higher specificity but lower
sensitivity.

Causes
A multitude of host, infectious, allergic, and environmental factors contribute to OM development.
Host factors
o Immune system: The immature immune systems of infants or the impaired immune
systems of patients with congenital immune deficiencies, HIV infection, or diabetes may
be involved in the development of OM. OM is an infectious disease that prospers in an
environment of decreased immune defenses. The interplay between pathogens and host
immune defense plays a role in disease progression. Patel et al (2009) found higher
interleukin (IL)6 levels in patients with OM who also had influenza and adenoviral
infections, whereas IL-1-beta (IL-1-beta) levels were higher in patients who developed
OM following URI.[2] In another study, Skovbjerg et al (2009) found that middle ear
effusions with culturable pathogenic bacteria were associated with higher levels of IL-1beta, IL-8, and IL-10 than sterile effusions.[3]
o Familial (genetic) predisposition: Although familial clustering of OM has been
demonstrated in studies that examined genetic associations of OM, separating genetic
factors from environmental influences has been difficult. No specific genes have been
linked to OM susceptibility. As with most disease processes, effects of environmental
exposures on genetic expression probably play an important role in OM pathogenesis.
o Mucins: The role of mucins in OME has been described. Mucins are responsible for gellike properties of mucus secretions. The middle ear mucin gene expression is unique
compared with the nasopharynx. Abnormalities of this gene expression, especially
upregulation of MUC5B in the ear, may have a predominant role in OME.
o Anatomic abnormality: Children with anatomic abnormalities of the palate and associated
musculature, especially the tensor veli palantini, exhibit marked ETD and have higher risk
for OM. Specific anomalies that correlate with high prevalence of OM include cleft palate,
Crouzon syndrome or Apert syndrome, Down syndrome, and Treacher Collins syndrome.
o Physiologic dysfunction: Abnormalities in the physiologic function of the ET mucosa,
including ciliary dysfunction and edema, increase the risk of bacterial invasion of the
middle ear and the resultant OME. Children with cochlear implants have a high incidence
of OM, especially chronic OM and cholesteatoma formation. One study described a
relationship between laryngopharyngeal reflux and chronic OM (COM); the authors
concluded that reflux work-up should be performed as part of COM investigations, and, if
reflux is confirmed, reflux treatment should be initiated in addition to treatment of primary
disease.[4]
o Vitamin A deficiency is associated with pediatric upper respiratory infections and AOM.
o Obesity has been linked to an increased incidence of OM, although the causal factor is
unknown. Speculations include alteration of intrinsic cytokine profile, increased
gastroesophageal reflux with alterations of the oral flora, and/or fat accumulation; all of
these have been linked with an increased incidence of OM. Conversely, OM may
increase the risk of obesity by altering the taste buds. [5]
Infectious factors
o Bacterial pathogens
The most common bacterial pathogen in AOM is Streptococcus pneumoniae,
followed by nontypeable Haemophilus influenzae and Moraxella catarrhalis.
These 3 organisms are responsible for more than 95% of all AOM cases with a
bacterial etiology.
In infants younger than 6 weeks, gram-negative bacilli (eg, Escherichia coli,
Klebsiella species, and Pseudomonas aeruginosa) play a much larger role in
AOM, causing 20% of cases. S pneumoniae and H influenzae are also the most
common pathogens in this age group. Staphylococcus aureus has also been
found as a pathogen in this age group in some studies, but more recent studies

suggest that the flora in these young infants may be that of usual AOM in children
older than 6 weeks.
Many experts had proposed that the MEE associated with OME was sterile
because cultures of middle ear fluid obtained by tympanocentesis often did not
grow bacteria. This view is changing as newer studies show 30-50% incidence of
positive results in middle ear bacterial cultures in patients with chronic MEE.
These cultures grow a wide range of aerobic and anaerobic bacteria; S
pneumoniae, H influenzae, M catarrhalis, and group A streptococci are the most
common.
M catarrhalis induced AOM differs from AOM caused by other bacterial
pathogens in several ways. It is characterized by higher a proportion of mixed
infections, younger age at the time of diagnosis, lower risk of spontaneous
perforation of the tympanic membrane, and an absence of mastoiditis. [6]
Further evidence for the presence of bacteria in the MEE of patients with OME
was provided by studies using polymerase chain reaction (PCR) assay to detect
bacterial DNA in MEE samples that were determined to be sterile using standard
bacterial culture techniques. In one such study using PCR assay, 77.3% of the
MEE samples had positive results for one or more common AOM pathogens (eg,
S pneumoniae, H influenzae, M catarrhalis).
In chronic suppurative OM, the most frequently isolated organisms include P
aeruginosa, S aureus, Corynebacterium species, and Klebsiella pneumoniae. An
unanswered question is whether these pathogens invade the middle ear from the
nasopharynx via the ET (as do the bacteria responsible for AOM) or whether they
enter through the perforated TM or a TT from the EAC.
The role of Helicobacter pylori in children with OME has been increasingly
recognized. Evidence that this agent might be responsible for OME comes from
its isolation from middle ear and tonsillar and adenoidal tissue in patients with
OME.
Alloiococcus otitidis is a newly recognized species of gram-positive bacterium
that has been recently discovered as a pathogen associated with OME. [7, 8] This
organism is the most frequent bacterium in AOM, as well as in OME. It has also
been detected in patients who had been treated with antibiotics, such as betalactams or erythromycin, suggesting that these agents may not be sufficiently
effective to eliminate this organism. Further investigation is needed to reveal the
clinical role of the organism in OM.

Viral pathogens
o Because acute viral URI is a prominent risk factor for AOM development, most
investigators have suspected a role for respiratory viruses in AOM pathogenesis.
o Many studies have substantiated this suspicion by showing how certain respiratory
viruses can cause inflammatory changes to the respiratory mucosa that lead to ETD,
increased bacterial colonization and adherence, and, eventually, AOM. Studies have also
shown that viruses can alter the host-immune response to AOM, thereby contributing to
prolonged middle ear fluid production and development of chronic OME.
o The viruses most commonly associated with AOM are respiratory syncytial virus (RSV),
influenza viruses, parainfluenza viruses, rhinovirus, and adenovirus.
o Human parechovirus 1 (HPeV1) infection is associated with OM and cough in pediatric
patients.[9] OM developed in 50% of 3-month follow-up periods that yielded evidence of
HPeV1 infection but in only 14% of the HPeV1-negative periods; in recurring OM, the
middle ear fluid samples were positive for HPeV in 15% of episodes.
Factors related to allergies
o The relationship between allergies and OM remains unclear. In children younger than 4
years, the immune system is still developing, and allergies are unlikely to play a role in
recurrent AOM in this age group. Although much evidence suggests that allergies
contribute to the pathogenesis of OM in older children, extensive evidence refutes the
role of allergies in the etiology of middle ear disease.

The following is a brief list of evidence for and against the etiologic role of allergy in OM:
Many patients with OM have concomitant allergic respiratory disease (eg, allergic
rhinitis, asthma).
Many patients with OM have positive results to skin testing or radioallergosorbent
testing (RAST).
Although mast cells are found in the middle ear mucosa, most studies fail to
show significant levels of immunoglobulin E (IgE) or eosinophils in the MEE of
patients with OM.
OM is most common in the winter and early spring, yet most major allergens (eg,
tree and grass pollens) peak in the late spring and early fall.
Most patients with concomitant OM and allergy show no marked improvement in
middle ear disease with aggressive allergy management, despite marked
improvements to nasal and other allergy-related symptoms.
Environmental factors
o Infant feeding methods
Many studies report that breastfeeding protects infants against OM. The most
recent and best of these studies indicates that this benefit is evident only in
children who are breastfed exclusively for the first 3-6 months of life.
Breastfeeding of this duration reduces the incidence of OM by 13%.
The protective effects of breastfeeding for the first 3-6 months persist 4-12
months after breastfeeding ceases, possibly because delaying onset of the first
OM episode reduces recurrence of OM in these children.
o Passive smoke exposure
Many studies have shown a direct relationship between passive smoke exposure
and risk of middle ear disease.
A recent systematic review of 45 publications dealing with OM and parental
smoking showed pooled odds ratios of 1.48 (95% confidence interval [CI] of 1.082.04) for recurrent OM, 1.38 (95% CI of 1.23-1.55) for MEE, and 1.3 (95% CI of
1.3-1.6) for AOM.[10]
o Group daycare attendance
Daycare centers create close contact among many children, which increases the
risks of respiratory infection, nasopharyngeal colonization with pathogenic
microbes, and OM.
Many researchers have used meta-analysis to confirm that exposure to other
young children (including siblings) in group daycare settings is a major risk factor
for OM.[11] A meta-analysis reported that care outside the home conferred a 2.5fold risk for OM. Other critical reviews of studies on OM and group childcare
show heightened odds ratios of 1.6-4.0:1 for center care versus home care.
Children who attend daycare centers frequently acquire antibacterial-resistant
organisms in their nasopharynx, leading to AOM that may be refractory to
antibacterial treatment. American Academy of Pediatrics and American Academy
of Family Physicians' guidelines recommend high-dose amoxicillin/clavulanic acid
as the antibiotic of choice in the treatment of AOM in children who attend
daycare.
Socioeconomic factors: Socioeconomic status encompasses many independent factors that
affect both the risk of OM and the likelihood that OM will be diagnosed. [12]
o In general, lower socioeconomic status confers higher risk for environmental exposure to
parental smoking, bottle-feeding, crowded group daycare, crowded living conditions, and
viruses and bacterial pathogens.
o Compared with children from middle-income and high-income families, children from
lower socioeconomic groups use health care resources less frequently, which decreases
the likelihood that OM cases will be diagnosed.
o

Differentials

Allergic Rhinitis
Apert Syndrome
Bacteremia
Cholesteatoma
Cleft Lip and Palate
Colic
Diarrhea
Down Syndrome
Fever in the Toddler
Fever in the Young Infant
Fever Without a Focus
Gastroenteritis
Gastroesophageal Reflux
Haemophilus Influenzae Infection
Head Trauma
Hearing Impairment
Human Immunodeficiency Virus Infection
Mastoiditis
Meningitis, Bacterial
Nasal Polyps
Nasopharyngeal Cancer
Otitis Externa
Otosclerosis
Parainfluenza Virus Infections
Passive Smoking and Lung Disease
Pharyngitis
Pneumococcal Infections
Primary Ciliary Dyskinesia
Respiratory Syncytial Virus Infection
Rhinovirus Infection
Sinusitis

Laboratory Studies

Laboratory evaluation is usually unnecessary, although many experts recommend a full sepsis
workup in infants younger than 12 weeks who present with fever and associated acute otitis
media (AOM).
OM is associated with multiple systemic diseases and congenital syndromes. AOM may be the
first presenting illness in some of these diseases; therefore, order appropriate laboratory studies
to confirm or exclude possible systemic or congenital diseases.

Imaging Studies

Imaging studies are not indicated in patients with OM unless intratemporal or intracranial
complications are suspected.
In patients in whom an OM complication is suspected, the imaging study of choice is a contrastenhanced CT scan of the temporal bones. CT findings help diagnose many complications (eg,
mastoiditis, epidural abscess, sigmoid sinus thrombophlebitis, meningitis, brain abscess, subdural
abscess). Finely cut CT sections through the temporal bone can reveal ossicular disease and
cholesteatoma. MRI is more helpful in depicting fluid collections, especially small middle ear

collections. MRI is usually performed following CT if further information is needed for definitive
diagnosis.

Other Tests

Tympanometry may help with diagnosis in patients with OME.

Some practitioners also use acoustic reflectometry to evaluate for MEE in patients with OM.

Procedures
In clinical trials, the criterion standard in the diagnosis of AOM is tympanocentesis to determine the
presence of middle ear fluid, followed by culture of the fluid to identify causative pathogens. Because of
the expense, effort, and lack of availability, no consensus guidelines call for routine use of
tympanocentesis to manage AOM and OME.
Tympanocentesis can improve diagnostic accuracy, guide treatment, and help eliminate
unnecessary medical or surgical interventions in selected patients with refractory or recurrent
middle ear disease.
Neonates, infants, and children with AOM who appear severely ill or toxic should undergo early
tympanocentesis with culturing. Children with acquired immunodeficiency virus (AIDS) or those
who are immunocompromised secondary to steroid therapy, chemotherapy, or
immunosuppressive therapy following organ transplantation should undergo early
tympanocentesis to exclude unusual organisms or nosocomial infection.
A recent report from the Centers for Disease Control and Prevention (CDC) working group on
drug-resistant S pneumoniae (DRSP) includes an option for tympanocentesis versus empiric
second-line antibiotic therapy in patients in whom initial antibiotic therapy has failed. [13]

Medical Care
Medical management of otitis media (OM) is actively debated in the medical literature, primarily because
of a dramatic increase in acute OM (AOM) prevalence over the past 10 years caused by DRSP and betalactamaseproducing H influenzae or M catarrhalis.
Beta-lactamases are enzymes that hydrolyze amoxicillin and some, but not all, oral cephalosporins,
leading to in vitro resistance to these drugs. Currently, 90% of M catarrhalis isolates and 40-50% of H
influenzae isolates in the United States produce beta-lactamases. As a result, empiric antibiotic therapy
for this disease has become more complex. Many opinions have been expressed regarding which drugs
are best for first- and second-line therapy or whether antibiotics should be prescribed in all patients with
AOM.

Guidelines for medical management of AOM

In 2004, the American Academy of Pediatrics and the American Academy of Family Practice published
guidelines for the medical management of AOM based on expert opinion and a thorough, nonsystematic
review of the literature.[14] Their recommendations are summarized as follows:
To diagnose AOM, the clinician should confirm a history of acute onset, identify signs of MEE, and
evaluate for the presence of signs and symptoms of middle-ear inflammation.
The management of AOM should include an assessment of pain. If pain is present, the clinician
should recommend treatment to reduce pain. Acetaminophen and ibuprofen are first-line drugs for
pain reduction.
OM is one of the most common disorders in children, and concern regarding antimicrobial
resistance due to aggressive antibiotic use is growing. Because of these concerns, treatment of
OM has significantly changed over the last decade. A growing number of physicians do not
recommend antibiotic prophylaxis or treatment in children with mild OM without a fever (or with
minimal fever). More importance is now given to observation and close follow-up.
Observation without use of antibacterial agents in a child with uncomplicated AOM is an option for
selected children based on diagnostic certainty, age, illness severity, and assurance of follow-up.

Many parents have concerns regarding this option, but education and involvement in medical
decisions increases acceptability.
Although instant access is available to clinical guidelines that recommend an expectant
management for children with OM who are older than 1-2 years, the antibiotic prescription rate is
still high in most emergency departments. If a decision is made to treat with an antibacterial
agent, amoxicillin should be prescribed for most children. When amoxicillin is used, the dose
should be 80-90 mg/kg/d.
In vitro antibacterial activity of amoxicillin against penicillin-susceptible and nonsusceptible S
pneumoniae strains isolated from children with AOM has shown that penicillin resistance cannot
be extrapolated to amoxicillin. Therefore, minimal inhibitory concentrations of penicillinnonsusceptible S pneumoniae for amoxicillin should be evaluated, and this antimicrobial agent
still remains a first-line choice for children with AOM.
If the patient fails to respond to the initial management option within 48-72 hours, the clinician
must reassess the patient to confirm AOM and exclude other causes of illness. If AOM is
confirmed in a patient initially treated with observation, the clinician should begin antibacterial
therapy. If the patient was initially treated with one or more antibacterial agents, the clinician
should change the antibacterial agent(s).
New alternative treatments for OM are desirable because of the relatively high prevalence of
recurrent and persistent AOM. The presence of the most prevalent etiologic agent, S
pneumoniae, especially penicillin-nonsusceptible strains in children, also supports alternative
treatment regimens.
Large-dose cefdinir therapy can be used in combination with tympanocentesis and has high
efficacy against penicillin-susceptible S pneumoniae.[15] The effectiveness is low for
nonsusceptible and H influenzae strains.
Clinicians should encourage the prevention of AOM through reduction of risk factors.
Evidence is insufficient to make a recommendation regarding the use of Complementary and
Alternative Medicine (CAM) for AOM.
Earlier recommendations from the American Academy of Pediatrics and the CDC working group on AOM
published in 1999 are summarized as follows:
First, distinguishing AOM from OME is critical. Prompt antibiotic therapy has been the
cornerstone of therapy for AOM for decades; however, antibiotics are not indicated for initial
treatment of OME.
Second, antimicrobials should not be prescribed in patients in whom AOM is only suspected or in
response to parental pressure on providers for specific therapy. A diagnosis of AOM should be
supported by a careful history and physical examination that document the presence of MEE and
concurrent signs or symptoms of acute illness (see History and Physical).
Third, patients with uncomplicated AOM who are younger than 2 years should be treated with a
10-day course of antimicrobials; children older than 2 years may be treated with a 5- to 7-day
course of antimicrobials. All patients with severe or recurrent AOM or with complications of AOM
should be treated for a minimum of 10 days.
Fourth, reserve antimicrobial prophylaxis for selected children with recurrent AOM. Recurrent
AOM is defined as 3 or more documented episodes within the prior 6 months or 4 or more
episodes in the preceding 12 months.
A meta-analysis of 6 randomized trials that studied the effects of antibiotic use in AOM showed that
children older than 2 years with mild AOM can be observed without the need for antibiotic administration.
[16]
Antibiotic administration seemed to have a beneficial effect in patients younger than 2 years with
bilateral OM and in patients with AOM and otorrhea.
A recent study determined the clinical practices related to the diagnosis of OM based on American
Academy of Pediatrics guidelines.[17] Authors reviewed 88 studies on OM diagnosis and treatment from
1994-2005. At least one American Academy of Pediatrics criteria were used in 81% of the studies,
whereas 20% of the studies used all 3 criteria. Use of these criteria can help provide uniformity to the
diagnosis and treatment of OM among various centers. The 2004 guidelines have also been shown to
reduce the rate of antibiotic prescribing practices among primary care physicians. [18]

Medical therapy for AOM

In 1999, the CDC therapeutic working group on DRSP published consensus recommendations for AOM
management.[19] The recommendations support the use of amoxicillin as the first-line antimicrobial agent
of choice in patients with AOM. The group recommended increasing the dose used for empiric treatment
from 40-45 mg/kg/d to 80-90 mg/kg/d because of concerns about increasingly resistant strains of S
pneumoniae, which are theoretically susceptible to this higher dose.
The recommendations for second-line therapy were more controversial, despite their reasonableness
from a scientific viewpoint. Stressing the importance of documenting true clinical failure of therapy after at
least 3 days of treatment with high-dose amoxicillin, the working group suggests tympanocentesis for
identification and susceptibility testing of the etiologic bacteria to guide alternate antibiotic therapy. In
cases in which second-line therapy is empirically chosen (a common occurrence, because few primary
care physicians routinely perform tympanocentesis in the office), the recommendations suggest
administering the following 3 preparations:
High-dose oral amoxicillin/clavulanate (80-90 mg/kg/d of amoxicillin component, 6.4 mg/kg/d of
clavulanate component)
Oral cefuroxime axetil (suspension: 30 mg/mg/d; tablet 250 mg bid)
Intramuscular (IM) ceftriaxone (administered as a single IM injection of 50 mg/kg on 3
consecutive days)
The choice of these 3 preparations from among the 16 antimicrobials currently approved by the US Food
and Drug Administration (FDA) for OM therapy was based on studies that reported that these drugs
achieve sufficient concentrations in middle ear fluid for bacteriocidal action against the common
pathogens in AOM, including DRSP and beta-lactamaseproducing H influenzae. Similar studies for the
other 13 approved agents either have not been completed or failed to show similar efficacy against
resistant bacteria.
These recommendations rely heavily on the pharmacodynamics model of drug efficacy. In this model,
clinical cure is believed to correlate with demonstrated penetrance of the antibiotic into the middle ear at a
level believed to be sufficient to kill the bacterial pathogens that cause AOM. Nevertheless, this model has
the following shortcomings:
Although bacteriologic eradication correlates with a successful clinical outcome, clinical success
occurs in more than 60% of patients, even when bacteriologic eradication is not achieved.
Eventually, almost all patients improve.
Validation of the pharmacodynamic model relies on tympanocentesis to identify the causative
bacteria and to measure antibiotic levels in middle ear fluid. Some antibiotics (eg, azithromycin
[Zithromax], clarithromycin [Biaxin]) concentrate intracellularly, not in middle ear fluid, and are
bacteriostatic, not bactericidal. A model predicated on certain drug levels and bacterial eradication
may underestimate the efficacy of these agents.
The drug levels used by the CDC to define bacterial killing were based on standards that
changed 6 months after the CDC publication.
The following crucial issues in AOM treatment were not clearly addressed by the CDC recommendations:
Patient compliance and the associated factors of dosing frequency, duration of therapy,
palatability, and drug cost
Guidance for special situations (eg, allergy to penicillins, beta-lactam drugs, or both)
Discussion of the option of withholding antibiotic therapy for 2-3 days in a subset of patients with
AOM who are likely to experience spontaneous resolution of disease with only supportive care
and analgesic therapy (a widespread practice in the Netherlands and Scandinavia but a practice
with few proponents in the United States)
Compliance, duration of therapy, and cost are important issues in treating children with AOM. The primary
determinants of compliance appear to be frequency of dosing, palatability of the agent, and duration of
therapy. Less frequent doses (ie, qd or bid) are more desirable than more frequent doses, which interfere
with daily routines. Shorter duration of therapy (ie, 5-7 d vs 10-14 d) increases compliance but should be
used only when equal clinical efficacy can be assured. In many instances, palatability ultimately
determines compliance in children.
For children who are allergic to penicillin or beta-lactam, the only currently available products are
cephalosporins, trimethoprim-sulfamethoxazole, or macrolides. Patients who are allergic to penicillin show
10-15% cross-reactivity when treated with cephalosporins. Levofloxacin has demonstrated higher efficacy

in the treatment of AOM when compared with amoxicillin/clavulanate and can be used in patients who are
allergic to penicillin.[20]
Pneumococcal resistance to trimethoprim/sulfamethoxazole is increasing and has become more
common than penicillin resistance in some areas. Use this drug to treat AOM only in regions
where it remains effective.
Of the macrolides, erythromycin/sulfisoxazole is a good choice, but many children refuse this
agent because of taste; a 5-day course of azithromycin or 10-day course of clarithromycin may be
preferred.
If DRSP is the suspected etiologic bacterium, do not use macrolides because pneumococcal
resistance is absolute with macrolides and, unlike the use of some beta-lactam antibiotics,
resistance cannot be overcome by increasing the dose.
Many children with AOM do not benefit from antimicrobial therapy, either because the etiology of the
illness is not bacterial or because their immune system clears the infection without use of a drug. No
clinical criteria currently distinguish which children do not require antibiotic therapy for AOM. Until such
criteria are available, many practitioners are unlikely to withhold initial antimicrobial therapy for proven
cases of AOM. Increasing awareness of the pathophysiology of the disease among parents and
healthcare providers has resulted in an increase in an observation-only approach in emergency
departments with less parental anxiety.[21]

Medical therapy for OME

Most cases of OME occur after an episode of AOM, and 67% of patients develop an MEE. The mean
duration of the effusions is 23 days, but many persist much longer. Most cases of OME spontaneously
resolve. Studies of the natural history of this disease report the following:
An MEE is harbored in 50% of ears 1 month after an episode of acute OME.
An MEE is harbored in 20% of ears after 2 months.
An MEE continues to be harbored in 10-15% of ears after 3 months.
OMEs that persist longer than 3 months have spontaneous resolution rates of only 20-30%, even
after years of observation.
Most cases of chronic OME are associated with conductive hearing loss, averaging approximately 25 dB.
Complications of hearing loss (eg, language delay, behavioral problems, poor academic performance)
have led to investigations of multiple medical and surgical treatments for OME. The following are among
the many strategies advocated for medical treatment in patients with OME:
Antimicrobials
Antihistamine-decongestants
Intranasal and systemic steroids
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Mucolytics
Aggressive management of allergic symptoms
Of these options, only antimicrobial therapy has provided measurable benefits. Steroid therapy (when
administered in combination with a beta-lactam antimicrobial) has shown benefit in some studies and no
benefit in others. All other medical therapies (ie, decongestants, antihistamines, mucolytics, NSAIDs)
have not provided measurable short- or long-term improvements in patients with OME.
Patients in whom OME is unresponsive to medical therapy and with an MEE that persists more than 12
weeks should be referred to an otolaryngologist to discuss surgical options in conjunction with further
medical therapies.
Antimicrobial therapy
o No clinical guidelines or consensus recommendations suggest which antimicrobials to
use as first-line agents for OME. In this era of increasing antibiotic resistance, selection of
an antibiotic agent should be individualized to the patient.
o In each patient, consider prior experience with antibiotics, age, sex, and daycare
attendance.
o If penicillin allergy is not a concern and if the patient has no recent exposure to
antibiotics, a reasonable choice for initial therapy is amoxicillin, administered at the same
high dose recommended by the CDC for AOM (ie, 80-90 mg/kg/d).

A reasonable first choice in a patient with antibiotic exposure during the prior month is
trial administration of a beta-lactamasestable agent (eg, amoxicillin/clavulanate) or a
second- or third-generation cephalosporin.
o As with antimicrobial selection, no recommendations have been made regarding duration
of therapy; 10 days is reasonable for amoxicillin, amoxicillin/clavulanate, and
cephalosporins. Studies of prolonged treatment in patients with OME show no advantage
in therapies that last longer than 10 days.
Steroid therapy
o The literature on steroid treatment is inconclusive. In 1994, the Agency for Health Care
Policy and Research (AHCPR) reviewed more than 5000 articles concerning the
management of OME and published a clinical practice guideline on the topic. [22] The
review reported that a combination of steroids plus antibiotics improved clearance of
MEE in 25.1% of patients. This difference did not meet statistical significance standards,
and the panel felt the risks of steroid administration outweighed potential benefits. The
final guideline states, "steroid medications are not recommended for treatment of OME in
a child of any age."
o Since publication of the AHCPR guideline, another investigation of steroids plus
antibiotics to treat OME has been published by Rosenfeld. [23] Rosenfeld reported that
surgery was avoided or postponed for 6 months in 1 of 4 children treated with steroids.
Therefore, steroid administration may have a role in patients who are not good surgical
candidates.
o The steroid regimen should be oral prednisone or prednisolone at a dose of 1 mg/kg/d for
5-7 days, administered in combination with a beta-lactam antibiotic.
o Steroids are contraindicated in patients with exposure to varicella who have not received
the varicella vaccine because of the possibility of life-threatening disseminated disease.
Controversy continues over the optimal management of OME. The AHCPR guideline, although criticized
for having a narrow scope, for favoring medical rather than surgical management of OME, and for
minimizing the problem of drug-resistant bacteria, provides a framework with which to consider
management options.
o

Surgical Care
From the beginning, integrate surgical management of AOM and OME with medical treatment for these
diseases. Early surgical interventions (eg, tympanocentesis) may be performed by primary care providers,
but more invasive procedures (eg, myringotomy, TT insertion, adenoidectomy) require an
otolaryngologist. In patients with intratemporal or intracranial complications of OM, surgical consultation is
critical. Certain special patient populations, such as those with cleft palate, Down syndrome, or other
craniofacial abnormalities, may require early surgical intervention to prevent OM.
Indications for tympanocentesis
o OM in patients who have severe otalgia, who are seriously ill, or who appear toxic
o Unsatisfactory response to antimicrobial therapy
o Onset of AOM in a patient receiving antimicrobial therapy
o OM associated with a confirmed or potential suppurative complication
o OM in a newborn, sick neonate, or patient who is immunologically deficient, any of whom
may harbor an unusual organism
Recommendations for TT insertion in children
o Chronic OME: TT insertion is recommended in children in whom OME is unresponsive to
a trial of antibiotic therapy and has persisted for at least 3 months, when bilateral, or at
least 6 months, when unilateral. In patients with unilateral OM, 6 months of persistent
OME is not an absolute indication for TT placement. If the patient has evidence of TM
structural abnormality secondary to OME or if the patient has recurrent infections, TT
placement is indicated. If these criteria are not met and hearing is normal in the affected
ear, careful observation is probably sufficient.
o Recurrent AOM: TT insertion is recommended in children with recurrent AOM, especially
when antimicrobial prophylaxis fails. A minimum frequency of 3 or more episodes of AOM

during the previous 6 months or 4 or more episodes (one of which is recent) during the
previous year indicates tube insertion.
o Recurrent OME: TT insertion is recommended in children with recurrent OME in whom
the duration of each episode does not meet criteria for chronic disease but cumulative
duration is considered excessive (eg, 6 of previous 12 mo).
o ETD: TT insertion is recommended in children with ETD (even in the absence of MEE) if
the child has persistent or recurrent signs and symptoms of ETD not relieved by medical
treatment options or if the child has ETD at the time of reconstructive middle ear surgery.
Signs and symptoms include hearing loss (usually fluctuating), disequilibrium/vertigo,
tinnitus, autophony, and severe retraction pocket.
o Barotrauma: TT insertion is recommended in children with barotrauma, especially for
prevention of recurrent episodes (eg, after air travel, hypobaric chamber treatment).
Adenoidectomy and/or tonsillectomy procedures performed to treat patients with OM (in addition
to myringotomy and TT placement) have generated extensive discussion and recent research,
although potential benefits are controversial. Current literature supports the following
recommendations from Bluestone:[24]
o Initial surgery: Myringotomy and TT placement are the initial surgical techniques (withhold
adenoidectomy unless the patient has a nasal obstruction). Some experts advocate
simultaneous adenoidectomy in patients older than 3 years because this has been shown
to improve ET function.
o Repeat surgery (following extrusion of tubes and recurrence of chronic MEE
unresponsive to antimicrobial therapy): Myringotomy, with or without tube placement, and
adenoidectomy, irrespective of adenoid size, are the techniques used.
o Tonsillectomy: Although it is not indicated for treatment of OM because it has not been
shown to benefit ET function, tonsillectomy may be performed concurrently with surgery
for OM if indications are present (eg, frequently recurrent tonsillitis, pharyngeal
obstruction).
Recommendations for surgery in patients with cleft palate, Down syndrome, and other
craniofacial abnormalities include the following:
o Myringotomy and TT placement are warranted in most children with cleft palate because
of inherent ETD and increased risk of OM. In patients who also have a cleft lip, the TT
may be placed at the time of initial lip repair, many months prior to palate repair. Consider
performing TT placement or replacement at the time of palate repair.
o Children with Down syndrome often exhibit ETD, conductive and sensorineural hearing
loss, EAC stenosis, and subtle immunologic deficiencies. These conditions create a high
risk for OM, make diagnosis of MEE difficult, and can lead to profound language and
learning difficulties.
The essential elements of care in these patients include close monitoring,
appropriate surgical interventions for EAC enlargement, and repetitive TT
placements.
Tube selection is a critical issue. These patients may require prolonged external
ventilation with TTs because of prolonged ETD. Unfortunately, TTs labeled as
long acting or permanent cause the greatest damage to the TM.
These patients often require repeated TT insertions, even when long-acting or
permanent TTs are used.
The best procedure may be to anticipate early extrusion and reinsertion and to
avoid these tubes in favor of ultrasmall TTs to prevent long-term TM damage.

Consultations

Otolaryngologist: Refer all patients who may require surgical interventions for complicated OM or
who have recurrent AOM or chronic OME to an otolaryngologist. Primary care physicians who are
uncomfortable performing tympanocentesis should refer patients who need this procedure to an
otolaryngologist.

Otologist: Children who present with subjective evidence of hearing loss should receive a formal
hearing test (ie, audiogram). Subjective evidence of hearing loss is often provided by a parent or
caregiver in younger children or, possibly, by a school teacher in older children.
Speech therapist: Speech therapy is indicated for patients in whom COM has caused speech and
language delays because of hearing loss.

Medication Summary

The FDA has approved more than a dozen antibiotics to treat otitis media (OM).
Some clinicians advocate administering corticosteroids in combination with a beta-lactamstable
antibiotic. Before prescribing such therapy, obtain a history of varicella, vaccination against
varicella, and recent exposure to a patient with varicella to avoid the risk of disseminated
varicella.
Studies of other adjunctive therapy for acute OM (AOM) and OME have shown that NSAIDs,
decongestants, and antihistamines provide no obvious benefits.

Antimicrobial agents
Class Summary
These agents remove pathogenic bacteria from middle ear fluid.

Amoxicillin (Biomox, Amoxil, Trimox)

Mainly bactericidal. As with penicillins, inhibits third and final stage of bacterial cell wall synthesis by
preferentially binding to specific PBPs located inside the bacterial cell wall.
PO semisynthetic aminopenicillin similar to ampicillin. Aminopenicillins are not stable in betalactamases of either gram-positive or gram-negative bacteria; more stable in gastric acid than
penicillin and more bioavailable than PO ampicillin.
Amoxicillin is associated with a lower prevalence of diarrhea than is ampicillin administered PO
because of the greater bioavailability of amoxicillin. Commonly used to treat infections (eg, OM,
bronchitis, sinusitis, bacterial cystitis) caused by susceptible organisms. To increase efficacy against
PRSP in OM or respiratory infections, higher dosing regimens have been recommended.

Amoxicillin and clavulanate (Augmentin)

As a beta-lactam antibiotic, amoxicillin is mainly bactericidal. Inhibits third and final stage of bacterial
cell wall synthesis by preferentially binding to specific PBPs located inside the bacterial cell wall. As
with all beta-lactam antibiotics, ability to interfere with PBP-mediated cell wall synthesis ultimately
leads to cell lysis.
Clavulanic acid is a beta-lactamase inhibitor that possesses weak antibacterial activity and acts as a
competitive "suicide" inhibitor of many plasmid-mediated and chromosome-mediated bacterial betalactamases.
Excellent choice for second-line therapy in AOM or initial therapy in OME. Drug combination treats
bacteria resistant to beta-lactam antibiotics. Combination with clavulanic acid reestablishes
amoxicillin's activity against beta-lactamase-producing bacteria. Excellent for treating infections due
to beta-lactamase-producing H influenzae and penicillinase-producing anaerobes.
Commonly used to treat infections (eg, AOM, acute sinusitis, acute bacterial cystitis, uncomplicated
gonorrhea, chancroid) caused by susceptible organisms.
For children >3 mo, base dosing protocol on amoxicillin content. Because of different
amoxicillin/clavulanic acid ratios in 250-mg tab (250/125) vs 250-mg chewable tab (250/62.5), do not
use 250-mg tab until child weighs >40 kg. Use the 7:1 formulation (ie, bid formulation) in higher doses
to minimize GI tract effects.

Cefaclor (Ceclor)
Second-generation PO cephalosporin indicated for infections caused by susceptible gram-positive
cocci and gram-negative rods. Has slightly improved activity against H influenzae compared to
cephalexin. Although marketed after first-generation agents, causing some clinicians to consider it a
second-generation agent, its spectrum more closely resembles first-generation cephalosporins.

Clinically, used primarily to treat OM, sinusitis, and URIs caused by H influenzae that are resistant to
ampicillin or amoxicillin.
Use higher doses for severe infections (eg, pneumonia, OM), less susceptible strains of pathogens,
and in patients who are obese.

Cefprozil (Cefzil)
PO, semisynthetic, second-generation cephalosporin. Binds to one or more PBPs, which, in turn,
inhibit cell wall synthesis and result in bactericidal activity. Possible second-line therapy for AOM or
initial therapy for OME. Therapeutic uses include OM, soft tissue infections, and respiratory tract
infections.

Cefuroxime (Ceftin)
Second-generation cephalosporin maintains the gram-positive activity of first-generation
cephalosporins and adds activity against Proteus mirabilis, H influenzae, E coli, K pneumoniae, and
M catarrhalis.
Common clinical uses include severe upper and lower respiratory tract infections, skin infections, OM,
and surgical prophylaxis.
Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose
and route of administration. Susp is less bioavailable than tab. Bioavailability is enhanced when
administered with food or infant formula.

Cefixime (Suprax)
Third-generation cephalosporin available in an PO formulation. As with ceftriaxone, has enhanced
antibacterial activity and increased stability against many beta-lactamases. By binding to one or more
PBPs, it arrests bacterial cell wall synthesis and inhibits bacterial growth.
Commonly used to treat OM, respiratory tract infections, and URIs caused by susceptible organisms.
When treating OM, susp is preferred due to higher serum concentrations achieved with this dosage
form compared with tabs.

Ceftriaxone (Rocephin)
Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against
gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by
binding to one or more PBPs. Has longest half-life of all cephalosporins, allowing once-daily dosing
and making it a useful antibiotic for outpatient therapy.
In Dec 1997, the FDA approved IM ceftriaxone to treat bacterial AOM caused by H influenzae (betalactamase negative), H influenzae (beta-lactamase positive), M catarrhalis (including beta-lactamase
producing strains), and S pneumoniae. Approval was based on the following data in children aged 5
months to 5 years: A prospective, randomized, double-blind, clinical trial compared the effectiveness
of a 50 mg/kg single dose of IM ceftriaxone (n=116) with a 10-d course of PO amoxicillin (n=117). The
authors concluded that a single IM injection of ceftriaxone is as effective as PO amoxicillin to treat
uncomplicated OM in children.
The CDC's DRSP therapeutic working group suggests this dose for 3 consecutive days in cases of
suspected resistant bacteria.

Cefpodoxime (Vantin)
Cefpodoxime proxetil is an PO prodrug for the extended-spectrum, semisynthetic, cephalosporin
antibiotic cefpodoxime. Spectrum is similar to third-generation cephalosporins and primarily has
gram-negative coverage but also covers some gram-positive organisms. Highly stable in the
presence of beta-lactamase enzymes; as a result, many organisms resistant to penicillins and some
cephalosporins (due to beta-lactamases) may be susceptible to cefpodoxime.
Indicated for treatment of upper and lower respiratory tract infections, UTIs, STDs, and skin and skin
structure infections. Has long half-life, allowing twice-daily administration. Approved by the FDA in
1984.

Clarithromycin (Biaxin)

PO macrolide antibiotic similar to erythromycin and azithromycin. Commonly used in infections of the
respiratory tract, STDs, OM, and infections in patients with AIDS. As with other macrolides, binds to
50S subunit of the 70S ribosome, thereby blocking RNA-mediated bacterial protein synthesis. Can be
bacteriostatic or bactericidal in action, depending on concentration and the particular organism and its
inoculum. Also penetrates phagocytes and macrophages efficiently, and, as a result, is effective
against a wide variety of organisms in respiratory infections.
Generally active against organisms that are usually susceptible to erythromycin, including most
staphylococcal and streptococcal strains. In addition, clarithromycin is active against M catarrhalis,
Mycoplasma pneumoniae, Legionella species, and Chlamydia pneumoniae. Beta-lactamase
production should have no effect on activity. Most strains of methicillin-resistant and oxacillin-resistant
staphylococci are resistant to clarithromycin.
Originally approved by the FDA in Oct 1991.

Azithromycin (Zithromax)
Semisynthetic antibiotic belonging to the macrolide subgroup of azalides. Similar in structure to
erythromycin. Inhibits protein synthesis in bacterial cells by binding to the 50S subunit of bacterial
ribosomes. Action is generally bacteriostatic but can be bactericidal in high concentrations or against
susceptible organisms.
Although significantly more expensive, it can be administered as a once-daily dose and produces less
GI tract intolerance than erythromycin. Apparent advantage over erythromycin is that it reaches
higher intracellular concentrations, thus increasing efficacy and duration of action. These advantages
are demonstrated in studies that show that single doses are effective for the treatment of STDs
caused by chlamydial and gonorrheal organisms.
Approved by FDA in Nov 1991. PO susp was introduced in Apr 1995. In late 1995, was approved for
treatment of pediatric OM and pharyngitis and, in mid 1996, was approved for MAC prophylaxis in
patients with advanced HIV disease.
IV form is also available for initial treatment of community-acquired pneumonia and pelvic
inflammatory disease.

Trimethoprim and sulfamethoxazole (Bactrim DS, Septra DS)

Also known as co-trimoxazole. Combination product of TMP and SMZ in a fixed 1:5 ratio. Ratio
produces serum concentrations of 1:20, which optimize antibacterial activity against some organisms.
Both TMP and SMZ are synthetic folate antagonists that are effective antimicrobials as individual
agents. TMP is usually bactericidal and acts by inhibiting sequential enzymes of the folic acid
synthesis pathway. SMZ is a structural analog of PABA and competitively inhibits formation of
dihydrofolic acid from PABA. TMP binds to and reversibly inhibits the enzyme dihydrofolate
reductase, which prevents formation of THF from dihydrofolic acid.
THF is a metabolically active form of folic acid. Without THF, bacteria cannot synthesize thymidine,
which leads to interference with bacterial nucleic acid and protein formation.
Combination of TMP with SMZ is synergistic against some bacteria. Usually active against
Staphylococcus epidermidis, S aureus, S pneumoniae, Streptococcus viridans, most
Enterobacteriaceae, Salmonella and Shigella species, H influenzae, M catarrhalis, and
Stenotrophomonas maltophilia.Enterococcus species, Neisseria gonorrhoeae, P aeruginosa, and
anaerobes are usually resistant or less susceptible. Also effective against Pneumocystis carinii,
Listeria monocytogenes, many Nocardia species, Yersinia enterocolitica, and Legionella
pneumophila.
Initially used in the treatment of UTIs but has since proved to be a versatile agent and is now widely
used in the prevention and treatment of P carinii pneumonia. Approved by FDA in 1973.

Erythromycin (E-Mycin, Eryc, Ery-Tab, Erythrocin)

Macrolide antibiotic produced by Streptomyces erythraeus; first of several macrolide antibiotics now
on the market.
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing
RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal

infections. Effective against wide range of microorganisms and, as with other antibiotics that inhibit
protein synthesis, is mainly bacteriostatic.
Activity against gram-positive organisms is usually greater than against gram-negative organisms
because of superior penetration into gram-positive organisms.
Gram-positive organisms susceptible to erythromycin include S aureus, Streptococcus agalactiae,
Streptococcus pyogenes, S pneumoniae, S viridans, and Corynebacterium diphtheriae. Gramnegative coverage is limited. In general, should not be used against H influenzae, although, in some
cases, organism may be susceptible. Although erythromycin is active against many microbes, its
clinical applications are relatively few.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is
desired, half of the total daily dose may be taken q12h. For more severe infections, double the dose.

Further Inpatient Care

Inpatient care is indicated only in patients with intratemporal or intracranial complications of otitis
media (OM).

Further Outpatient Care

Most acute OM (AOM) cases resolve with antibiotic therapy, but recurrences are frequent. By the time
children are aged 7 years, more than one third have experienced 6 or more episodes of AOM. In
addition, many patients who are treated for AOM subsequently develop asymptomatic OME.
Monitoring by otoscopic examination, acoustic reflectometry, and/or tympanometry is necessary to
determine which children require further follow-up care and therapy to prevent hearing loss and
resultant speech and learning disabilities.
Although the precise timing of follow-up visits is a matter of debate, examination after 4-6 weeks is
reasonable. At the 4-week to 6-week follow-up visit, children in whom OME has not resolved should
be rescheduled for a second follow-up appointment 4-6 weeks after the first.
If effusion persists as long as 12 weeks, perform a hearing test.
Refer any child in whom the hearing loss in both ears exceeds 20 dB for surgical treatment with a
bilateral myringotomy and TT placement.
Children with a hearing loss of less than 20 dB and an MEE that persists beyond 12 weeks can be
monitored, with the understanding that significant spontaneous improvement of the MEE after 12
weeks is unlikely, or they can receive antibiotic therapy using a beta-lactamstable agent.

Inpatient & Outpatient Medications

Antibiotics eradicate bacteria in the middle ear that cause the inflammatory response leading to MEE
and the symptoms of AOM (see Medication). The most common bacteria are S pneumoniae, H
influenzae, and M catarrhalis.

Deterrence/Prevention
Medical strategies to prevent OM include eliminating risk factors for AOM, immunologic interventions, and
antibiotic prophylaxis. Surgical strategies to prevent recurrent OM include prophylactic myringotomy and
TT insertion.
Risk factors: These include daycare attendance, secondary exposure to tobacco smoke, pacifier
use, and breastfeeding for less than 3 months (breastfeeding >3 mo decreases risk).
o Daycare attendance
A recent meta-analysis of studies of risk factors for AOM reported care outside
the home increases the relative risk of recurrent AOM by approximately 2.5 fold,
probably due to greater exposure to respiratory infections. Children in daycare
have an increased frequency of URIs, and their infections are often more
prolonged.
AOM risk correlates with the number of contacts with other children rather than
the absolute number of children enrolled in a center. Rates of respiratory

infections, including AOM, are higher among children in daycare centers than
among those receiving family care.
The risk of increased infection associated with group daycare is greatest in the
first 2 years of life and particularly in the first year.
o Tobacco smoke exposure
Tobacco smoke is an upper respiratory irritant, and multiple studies have shown
that passive smoke exposure places children at increased risk for pneumonia,
bronchitis, bronchiolitis, chronic MEE, and more frequent and severe asthma.
Most of the prior controversy regarding the relationship between tobacco smoke
exposure and OM resulted from faulty study design and a failure to objectively
quantify tobacco smoke exposure. Studies have controlled for confounding
factors more carefully, and many have measured serum or urine concentrations
of cotinine, a nicotine metabolite, to objectively determine exposure to passive
tobacco smoke. These studies consistently establish a direct relationship
between parental smoking and increasing risk of AOM.
A recent meta-analysis of risk factors determined that parental smoking
increases the risk of AOM by 66%. The average duration of MEE in children with
elevated cotinine levels was 28 days, compared with 19 days' duration in children
without elevated levels.
o Pacifier use: This clearly increases the risk for AOM in infants and small children,
although the reason for this predisposition is uncertain. In one study, the relative risk for
recurrent AOM was 1.6 in children younger than 2 years who used a pacifier and 2.9 in
children aged 2 and 3 years who used a pacifier. According to one theory, the constant
sucking action associated with pacifier use exacerbates ETD, leading to inoculation of the
middle ear with pathogenic bacteria.
o Breastfeeding for a duration of less than 3 months
Breastfeeding protects young infants from OM and GI tract illness. A recent metaanalysis reported that breastfeeding for at least 3 months resulted in a relative
AOM risk of 0.87 and a relative risk of recurrent AOM of 0.69. Breastfeeding for
at least 6 months reduced the risk of AOM even further.
The risk reduction probably results from transferred immunoglobulins, cellular
elements, and many nonspecific components in mother's milk that, collectively,
exhibit antibacterial, antiviral, and antiparasitic properties.
Passive and active immunizations
o Passive immunization with RSV immunoglobulin IV (RSV-IGIV) in selected infants
Prophylactic administration of RSV-IGIV before the beginning of the RSV season
(ie, Oct-Dec) prevents serious lower respiratory infections and significantly
reduces episodes of AOM in selected pediatric populations (ie, children < 2 y with
bronchopulmonary dysplasia who have required oxygen therapy within the 6 mo
prior to the RSV season, infants born before 32 weeks' gestation).
The cost of this therapy is prohibitively high. A recent study reported that the cost
of RSV-IVIG therapy in early 2001 was approximately $7000-$8000 per episode
of AOM prevented.
RSV-IGIV immunization cannot be recommended beyond the specific population
described above, and even then, can only be recommended to prevent lower
respiratory infections rather than as prophylaxis for AOM.
o Pneumococcus vaccine
In February 2000, the FDA approved use of heptavalent pneumococcal CRM197
conjugate vaccine (PCV7), marketed under the brand name Prevnar by Wyeth
Pharmaceuticals. PCV7 is composed of 7 pneumococcal antigens (ie,
polysaccharide serotypes 4, 6B, 9V, 14, 19F, 23F; oligosaccharide serotype
18C), conjugated to 20 mcg of CRM197 by reductive amination.
The recommended primary series is 3 doses administered at ages 2, 4, and 6
months, with a minimum of 6 weeks between doses. A fourth (booster) dose is

recommended at age 12-15 months or at least 60 days after completion of the

primary series. PCV7 provides potential serotype and serogroup cross-protection
(eg, 6A) in 88% of cases of bacteremia, 82% of cases of meningitis, and 71% of
cases of pneumococcal OM episodes in children younger than 6 years in the
United States.
PCV7 had decreased the number of episodes of S pneumoniae AOM caused by
the serotypes included in the vaccine. It had reduced the nasopharyngeal
carriage of vaccine-type S pneumoniae, particularly antibacterial-resistant
organisms, and had also prevented the spread to contacts in the community. A
recent observation of increased rates of antibacterial-resistant nonvaccine
serotype S pneumoniae may erode the success of PCV7.
Since the initiation of the heptavalent pneumococcal vaccine in 2000,
researchers have found that nearly two thirds of invasive pneumococcal disease
cases in young children have been caused by 6 serotypes not covered by that
vaccine. Those serotypes, along with the original 7, have been incorporated into
pneumococcal vaccine valent-13 (Prevnar 13), which was approved in February
2010.
Pneumococcal polysaccharide vaccines have been recommended since 1985 for
children older than 2 years who are at high risk for invasive disease, but these
vaccines were not recommended for younger children and infants because of
poor antibody response in children younger than 2 years.
Prymula et al have described the effectiveness of a new vaccine that contains
pneumococcal capsular polysaccharides conjugated to H influenzae derived
protein D in the prevention of a first episode of AOM. [25] According to their data, at
present, the full effectiveness of the vaccine in treating children is questionable,
even in high-risk children.
Pneumococcal conjugate vaccines, such as PCV7, induce proposed protective
antibody responses (>0.15 mcg/mL) in more than 90% of infants after a series of
3 doses administered at ages 2, 4, and 6 months. Following the priming doses,
significant booster responses (ie, immunologic memory) are apparent when
additional doses are administered in patients aged 12-15 months. In efficacy
trials, this new vaccine was associated with a 7% decrease in OM and a 15-20%
decrease in TT placement.
Most antibiotics are effective in treating AOM despite changed microbiology due
to the use of PCV7.[26]
o Influenza vaccine
Influenza is a highly infectious viral illness that is common during the winter
months. A small proportion of AOM is directly caused by influenza viruses and
may be directly prevented by immunization with influenza vaccine. In addition,
any influenza infection of the upper respiratory tract leads to respiratory epithelial
inflammation and associated ETD, which predisposes the host to bacterial AOM.
Influenza vaccine is strongly recommended for any person older than 6 months
in whom age or an underlying medical condition creates increased risk for
complications of influenza.
Influenza vaccine can be administered to any person who wishes to reduce the
chance of infection by the virus. The vaccine can be administered to children as
young as 6 months. Many experts recommend that children who are prone to OM
receive the annual vaccine, particularly those in group daycare who have
increased risk of URIs and AOM.
Antibiotic prophylaxis
o Many studies in the 1970s and 1980s showed the effectiveness of antibiotic prophylaxis
in children with recurrent AOM. The most common regimens were sulfisoxazole (35
mg/kg/dose qd or bid) or amoxicillin (20 mg/kg/dose qd or bid). These therapies were
usually administered in patients who had 3 or more episodes of AOM within a 6-month
period or 4 or more episodes within 12 months.

The use of antibiotic prophylaxis for AOM has become widely questioned because of the
increasing antibiotic resistance among bacterial pathogens responsible for middle ear
infections. Even before the drastic rise in drug-resistant bacteria, the clinical effectiveness
of antibiotic prophylaxis for AOM was unimpressive.
A meta-analysis of 1993 studies showed that a child must be treated for 9 months to
prevent just one episode of AOM.[27] The meta-analysis was based on decade-old data
that are almost irrelevant now because of the new prevalence of drug-resistant bacteria.
Most experts who supported antibiotic prophylaxis no longer recommend routine
antibiotic prophylaxis for all children with recurrent AOM.

Complications

Mastoiditis
o Mastoid infections have 2 forms, namely, acute coalescent mastoiditis or chronic
mastoiditis with osteitis. Treatment for both types of mastoiditis is a mastoidectomy.
o Acute coalescent mastoiditis occurs when obstruction of the aditus (the small opening
between the epitympanum and the mastoid antrum) creates a sealed space in the
mastoid antrum (the air space in the mastoid portion of the temporal bone that
communicates with the tympanic cavity and mastoid air cells). Acute infection of the fluid
in this space usually occurs as an extension of middle ear infection. Diagnosis is
confirmed with a CT scan of the head that reveals loss of septation between mastoid air
cells.
o Chronic mastoiditis occurs when acute mastoiditis remains undetected, with subsequent
changes in the mucosal lining of the mastoid air cells. Granulation tissue filled with
inflammatory cells replaces the air spaces of the mastoid and middle ear, and bone
necrosis with erosion may result, leading to an extracranial Bezold abscess (see image
below) or intracranial complication. Chronic mastoiditis may not be depicted on CT scans.
MRI reveals regions of nonspecific bright signal, consistent with inflammation.

Acute coalescent mastoiditis with a Bezold abscess in

a young girl who presented with chronic right ear pain and multiple untreated middle ear
infections.
Cholesteatoma
o Cholesteatomas are cystlike expanding lesions of the temporal bone, lined by stratified
squamous epithelium and containing desquamated keratin and purulent material. The
etiology of cholesteatoma is controversial. Although cholesteatoma development is
complicated and incompletely understood, contributing factors include ETD, increased
negative pressures in the middle ear, repeated infection, chronic MEE, loss of collagen
fibers and structural support of the TM, collapse of the TM, and formation of chronic
retraction pockets.
o Diagnosis is difficult but can be made by an experienced clinician using a pneumatic
otoscopic examination in patients with chronic middle ear disease and progressive
conductive hearing loss.
o Treatment is surgical excision or exteriorization. In very rare cases (eg, the patient is not
a surgical candidate because the cholesteatoma is secondary to a comorbid disease),
repeated cleansing under a surgical microscope may temporarily control the
cholesteatoma.

Labyrinthitis
o Inflammation of the labyrinth produces vestibular and auditory symptoms. In patients with
COM, bacteria may infiltrate the bony labyrinth and produce a condition of suppurative
labyrinthitis. Acute symptoms include hearing loss and vertigo, which usually improve
after the body goes through a phase of central compensation for the damaged vestibular
organs. Prolonged labyrinth infection leads to vestibular end-organ damage and
permanent hearing loss.
o Diagnosis of labyrinthitis in patients with COM is most often retrospectively confirmed.
Vertigo and sensorineural hearing loss in these patients is presumptive evidence for
labyrinthitis.
o In patients in whom hearing or vestibular function recovers, labyrinthitis is classified as
serous rather than suppurative; recovery indicates that the bacteria never truly invaded
the labyrinth and that the symptoms were caused by severe inflammation of the
vestibular organs without bacterial invasion.
o Labyrinthitis treatment includes intravenous antibiotics directed against the common
pathogens in COM to limit damage to vestibular organs. Vestibular suppressants are
used in the acute period to relieve dizziness and nausea.
Facial paralysis
o In patients with invasive OM (especially OM with cholesteatoma), infection and
inflammation of the facial nerve leads to edema and nerve fiber compression that causes
facial paralysis. The facial nerve courses through the temporal bone in the fallopian
canal, protected by bone and epineurium. Naturally occurring bony dehiscences of the
fallopian canal and reactive osteitis (often due to cholesteatoma) place the facial nerve at
risk in invasive OM.
o The combination of OM with concurrent ipsilateral facial paralysis suggests an obvious
diagnosis, but other entities in the differential diagnosis for acute facial paralysis should
be considered. Treatment is immediate administration of intravenous antibiotics and/or
surgical treatment of the cholesteatoma involving the facial nerve.
Meningitis
o Meningitis is among the most common intracranial complications of OM, occurring in
children with either AOM or COM.
o Fever accompanied by neck stiffness should immediately prompt a search for an
intracranial complication. As with all intracranial complications, perform a contrastenhanced CT scan or MRI.
o Lumbar puncture and examination of the CSF is mandatory in patients in whom
meningitis is suspected. CSF leukocytosis, with low glucose and high protein and lactate
levels, is characteristic of meningitis. Studies of the CSF should include Gram staining,
culturing, and testing for bacterial antigens.
o The treatment of choice is immediate administration of broad-spectrum intravenous
antibiotics, followed by directed therapy based on CSF culture results. Some experts
have reduced neurologic and auditory sequelae resulting from meningitis by
administering dexamethasone early in the treatment course.
Epidural abscess
o Epidural abscesses secondary to OM occur near the temporal bone. Infection extends to
the epidural space through venous channels in the bone or by bone erosion. The most
common routes for extension are through the thin bone of the tegmen to the middle
cranial fossa or through the bone adjacent to the sigmoid sinus and posterior cranial
fossa.
o Most intracranial complications are accompanied by a concomitant epidural abscess
because of the pathways involved in OM spread.
o Diagnosis relies on high clinical suspicion and is confirmed using contrast-enhanced CT
scan or MRI.
o Treatment requires surgical exploration, with a cortical mastoidectomy and thinning of the
bone overlying the tegmen tympani, sigmoid sinus, and posterior fossa to allow the

epidural space to be seen. If granulation tissue or purulent fluid is discovered in the

epidural space, continue removing bone until noninflamed dura is encountered.
Lateral sinus thrombophlebitis
o Lateral and sigmoid sinuses are relatively unprotected from direct extension of infections
from the middle ear and mastoid. Direct extension occurs secondary to bone erosion
from osteitis or necrosis. Indirect extension occurs via retrograde thrombophlebitis of the
mastoid emissary veins.
o Obstruction of venous drainage by thrombosis can produce elevated intracranial pressure
(ICP) and headache. Otitic hydrocephalous can complicate the course of lateral sinus
thrombosis, leading to vision changes and sixth cranial nerve (CN VI) palsy. Septic
emboli can disseminate the infection to distant body sites, and the constant bacteremia
produces febrile episodes.
o The classic clinical picture of high spiking fevers, headache, and active ear disease is
rare. Diagnosis of this complication relies on high clinical suspicion and is confirmed by
MRI or contrast-enhanced CT scan demonstrating the thrombosis.
o Early administration of intravenous antibiotics and surgical exploration are the mainstays
of therapy. After exposing the sigmoid sinus, a needle may be used to aspirate the sinus.
If free-flowing blood returns, no further surgery is needed. If no blood returns, open and
drain the sinus.
Brain abscess
o Brain abscess is the first or second most common intracranial complication of COM. Most
abscesses form in the temporal lobe or cerebellum, supporting the theory that brain
abscesses associated with OM are probably caused by direct extension of infection and
not hematogenous spread of bacteria.
o In addition to fever from the infectious process, symptoms and signs of brain abscess
relate to abscess location and the overall mass effect of the abscess. Headache,
vomiting, and lethargy may indicate increased ICP. Significant localizing signs include
seizures, hemiparesis, cranial nerve palsies, and aphasia. Abscesses in the temporal
lobe or cerebellum can exist with relatively few early localizing symptoms.
o A contrast-enhanced CT scan or MRI is the diagnostic study of choice.
o The initial therapy of choice is administration of broad-spectrum antibiotics. Consult with
a neurosurgeon for decisions about abscess drainage. In some patients, mastoid surgery
can be performed with a neurosurgical procedure. Otologic surgery can be delayed in
patients who are less stable until neurologic stability is established.

Prognosis

The prognosis for almost all patients with OM is excellent; the exceptions are patients in whom
OM involves intratemporal and intracranial complications (< 1%).
Data on cognitive and educational outcomes of OM in the literature are limited. The impact of OM
on child development depends on numerous factors. OM in infants younger than 12 months
predisposes to long-term speech and language problems. OM has also been reported to
negatively affect pre-existing cognitive or language problems. Careful follow-up and early referral
are key to management.

Patient Education

Patient education topics should include the following:

o Avoiding risk factors
o Appropriate use of antibiotics
o Understanding the implications of antibiotic-resistant bacteria in OM
Education for health care providers should focus on the following topics:
o Antibiotic-resistant bacteria and the need to avoid overprescribing antibiotics
o Importance of pneumatic otoscope examination to distinguish AOM from OME

Treatment differences between AOM and OME